An autoimmune disease is generally described as a chronic condition in which the immune response targets molecules associated with healthy cells and tissue. In an autoimmune disease, some component of the immune system interferes with normal cell functions. Also, the ability to repair the damaged tissue cannot keep pace with the rate of tissue destruction.
An estimated 18.2 million people in the US have diabetes, which is now considered to be an organ-specific autoimmune disease. Further, it is estimated that 5.2 million have not been diagnosed. Type 1 diabetes accounts for 5-10% of the cases of diabetes; i.e., about 1.8 million people. In 2002, diabetes cost the US $132 billion: $40 billion in indirect costs-lost wages, premature death, disability payments, and $92 billion in direct costs. Risks for developing Type 1 diabetes include genetic predisposition and possible environmental factors.
In the pancreas, the islets of Langerhans contain several cell types that secrete distinct hormones. Each cell type expresses different tissue-specific proteins: a cells express glucagon; β cells express insulin; and, δ cells express somatostatin. In insulin-dependent diabetes an effector T cell recognizes peptides from a β cell-specific protein and kills the β cells. Glucagon and somatostatin are still produced by the α and δ cells, but no insulin can be made.
Type 1 diabetes is mediated by autoreactive T cells that induce inflammations in the pancreatic islets and selectively destroy the insulin-producing β cells in the pancreas. The immune-mediated destruction of insulin-producing cells in the pancreas leads to dangerously high levels of glucose in the blood. There is a need to be able to control the pathogenic activities of islet-specific T cells to ameliorate the onset and progression of Type 1 diabetes.
Also, there is a need to be able to control the pathogenic activities of such islet-specific, T cells to provide protection from recurrent diabetes in individuals receiving islet transplants.